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Caution: This is a fairly lengthy article . Optimal Reading time  15  minutes

Cardiac failure is a progressive systemic disease  ,  even though the primary problem originates in the heart .Most of the symptoms and clinical features are related to Neuro-Endocrine activation instigated by poor pumping function.When the diminishing cardiac function exceeds the compensatory mechanisms , full blown cardiac failure sets in and get into a vicious downward spiral unless  intervened.

The conventional treatment model involves  on three targets.

  • Reduction in pre -load(Diuretics)
  • Improving  contractility (Inotropics)
  • Reduction in afterload  (Vaso- dilators)

Though the concept looked attractive  there are many missing links . Medical treatment   lags far  behind  the desired goals. Still , it  can stabilize most of the patients with cardiac failure till they reach very late stages.

Nomenclature

Inadequately  treated  CHF is not  synonymous  with refractory failure  . But  ,  practically it is the commonest cause for refractionaries . Hence  , every patient must be scrutinised meticulously for adequacy of treatment.

Primary mitral  , aortic valve  lesions causing cardiac failure need  not be considered as refractory  cardiac failure . In the strict sense myocardial disease /damage  either  idiopathic or secondary to CAD  would form  bulk of refractory failure .

(For example a patient with critical aortic stenosis with severe LV dysfunction is   technically  refractory cardiac failure but functionally it could be a  simple  expression of  after load mis- match )

COPD -Cor pulmonale /Primary pulmonary  hypertension  / End  stage congenital  heart disease  and   Eisenmenger syndromes   form separate  group of  CHF and would not be discussed  here.

The valves , the fibrous skeleton, the  pericardium are integral parts  of the heart . Individual disease process can affect these compartments in a differential pattern .

When we  refer to  refractory heart failure   it amounts only two  large disease groups.Ischemic and idiopathic  cardiomyopathy.The whole myocardium is a single unit. If it is destined to fail  it will fail in toto.  There can be reversible factors that can be addressed.

The coronary artery   though not a part of heart has a major say in the outcome of cardiac failure as they determine the cardiac muscle  integrity.In every patient with refractory cardiac  failure , an attempt must be made to rule out  any  re-vascularisible  lesions.

The primary difference between ischemic and Idiopathic DCM   is ,  in ischemic DCM left ventricular  segments  are predominantly involved . RV function  is relatively   preserved until very late stages.

Patient factors

Age , gender, body weight , systemic illness that increase metabolic demands have an adverse impact . Diabetic patients fare poorly .

Fluid management  and  diuretics

In refractory cardiac failure the renal blood flow is reduced .Diuretics usage will further worsen this if ECF is depleted .

So it is obvious we have to use it very judiciously .

Why only  certain patients with cardiac  failure   develop significant edema while others do not ?

This lies in the response of neuro -humoral  activation of secondary RASS system.

Both inadequate  and excess diuretic can perpetuate the  status.

Intra vascular hypovolemia and effective renal blood flow reduced

Diuretic strategies

  • Increasing the dose
  • Adding another ( Switching over to another loop diuretic like Bumetanide, or Toresemide  can be tried )
  • Sequential nephron blockade ( Add  metalazone a powerful thiazide acting in proximal tubule  to be used with caution risk of hypokalemia)
  • Continuous IV infusion  is an option

Ultra filtration  can be  used  in severely volume over loaded  patients.

Refractory diastolic failure .  How common is that ?

The incidence of significant LV filling defect are more commonly observed.There is no specific  drugs  available to tackle this .It may be argued digoxin and other positive inotropes worsen diastolic dysfunction.This  may not be true in the bed side.Unless severe  LV restriction feature are present  digoxin can be continued.

The simple and effective way to improve LV filling in the presence of diastolic filling defect ,  is to slow down the heart rate. At low heart rates  diastolic filling period prolongs and dysfunction tend to vanish.Beta blockers usefulness  in   DCMs  is attributed to this phenomenon

Specific  therapeutic targets

RV dysfunction

RV dysfunction is responsible for systemic congestion .RV function improvement alone can improve the functional class in  many .Controlling and targeting pulmonary hypertension is beneficial . There can be a role for off  label use for chronic pulmonary hypertension associated with DCM.

Importance of  weight reduction :

We can comprehend  complex equations  in  cardiac failure  , still we often  forget a simple logic  . Body wieght is an  indirect but powerful determinant of aortic after load.  A 80kg body needs more heart power than a  body with a 40 kg  mass. If a  patient with EF of  25 %  loses 50 % of his body mass,   his heart can serve  his body  for   100 % longer duration.   (Of course ,  this happens  in certain patients  by a mechanism  called  cardiac  cachexia !  shall we call  it as  natural adaptation ?  )

 Inflammation   control

Tumor necrosis factors and Interleukins are responsible for systemic reaction . These levels are high in CHF. Anti -Inflammatory drugs and diet would help. Statin usage is shown to be beneficial.

Metabolic modulation

ATPs ,fatty acid are fuels for the  heart .Ailing hearts  require  it in plenty. Certain drugs like Trimetazidine, L carnitine has been shown to be useful .

Cardio-Renal syndrome

This is nothing but raising renal parameters  as heart failure worsen .This  essentially  involves fluid and electrolyte management.

Natural course of refractory cardiac failure

It is sort of a  delayed near death sentence . 5 year survival is comparable to many cancer inflicted patients.Basic medical care  remain the corner stone. CRT /ICD*  , LV  assist devices are slightly more effective with substantial  risks and cost involved. Indicated only for  rich  and  insurance infested  population who can tolerate both scientific and  financial excesses.

ICDs* do prevent sudden electrical deaths.

 There is a  fundamental flaw  of  electrical and mechanical device concepts  in refractory heart failure .It  forgets  ,  CHF is a  systemic disease .A  cardio centric approach rarely works to perfection .

Cardiac transplantation  is the ultimate . It works well beyond any doubt. In best centers  like  Stanford 85 %   for 5 year survival is expected. Heart transplantation is limited by donor  availability and  surgical infra structure.Total artificial heart is a distant dream , but will be definitely accomplished

Role of surgery

CABG ( Strictly Indicated only in absolutely deserving .The habit of  revascularising scarred, akinetic DCMs to be abandoned )

Ventricular reduction( Batisda -seems to work only in Brazil!)

Mitral valve  interventions

Some  exotic interventions in cardiac failure

Mitral splinting to  reduce secondary mitral regurgitation in DCM

 

Newer drugs  and experimental drugs

Nesiritide, (Synthetic Brain naturetic peptide )  Tolvapton ( Vasopressin antagonist) are used with varying  success .


20  point bed side prescription tips  for refractory failure.


  1. Correct the  underlying causes  and triggers.Try to correct any  critical coronary lesion if any by PCI /CABG ( Not a major game changer ! )
  2. Restrict activities (Better to remain in class 3)
  3. Admit  only if  persistent  class 4 .(Intermittent class 4 does not require admission )
  4. Do not try vigorously to move up to class 2  with inotropes  you may  end up in class 4 !
  5. Advice mild passive and active movements. (6 minutes walk > 300 -400meters)
  6. Educate the entire  family / Ask them to shun Internet  (Internet acquired half baked medical knowledge is more injurious to health )
  7. Restrict salt intake
  8. Continue  Digoxin till toxicity develop  or maximum  dose  is reached  (Milrinone /Amrinone make  no major difference )
  9. Optimse diuretics.  Add Metalazone to Frusemide.
  10. Maintain good hemoglobin level (Erythropoitin does not work !)
  11. Add beta blockers  in every one including many of the  class 4 (Not necessarily Carvidilol)
  12. ACEI remain a key drug . Titrate to maximum tolerated dose. (Additional ARBs not much useful)
  13. Aldosterone antagonist has  unique role (Anti-fibrotic ? )  Caution required in diabetic patients  in monitoring renal function .
  14. At-least One metabolic modulator like  Trimetazide  could be tried (ATP utilisation amplified)
  15. Fatty acid metabolism enhancer  L carnitine  may be useful (Recall 1st year medical school basics  . . . Heart thrives on fat energy more  !)
  16. Nephrologist consult  is recommended if electrolyte / ECF status fluctuations are more.
  17. Avoid dobutamine infusions unless patient  insist.
  18. Narcotics like morphine can be used liberally in terminal heart failure  (Both for hemo-dynamic  and  neural benefits )
  19. As far as possible do not send these  patients  to big tertiary hospital unless heart transplantation is planned.
  20. Don’t  be a party  in  exhausting the  personal finance resources of the patient by ordering exotic investigations . Let him not suffer from additional worry ! (By the way . . .  having a hefty health insurance limit  is not an excuse  . Depleting  it  for futile purposes   would make the national economy weaker ! )

Final message

 Three  principles of  management in  refractory  cardiac failure  

  1.   Systemic approach  is the key .
  2.   De-mystifying   cardio centric  interventions  is essential.
  3.   Psychological support is vital .

Functional capacity   has a  poor correlation with LV contractile function . The skeletal  muscle  integrity , blood flow , and its  metabolism has critical say in this. Optimal medications  , properly regulated  locomotion  , weight reduction   can have a major impact.

The secrets of living a good quality of life    in  cardiac failure   ,  lies  not in modern technology  but in the  rare commodities  called  common sense and compassion.

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We now understand , heart rate reduction  could be the single most important factor  in the management of heart failure .Beta blockers have proved this time and again.We know heart rate has a linear relationship between survival .

SHIFT trial has  proven  that  Ivabradine  has a major role in the management  of chronic heart failure therapy .It is an If current blocker .  No hemodynamic  side effects was noted.

How does Ivabradine act ?

It acts on the phase 4 diastolic depolarisation in SA node by slow I f  currents.

SHIFT trial Link to lancet

SHIFT study official website

In this trial , the usage of  optimal Beta blockers  was  only in 25 %  . Patients  who received   complete beta blockade did show much benefit with Ivabradine . Further, the usage of  digoxin was only around 20% .This does not represent  the realistic  population of  cardiac  failure in many  countries  .In India , almost 70-80 % receive  it . Digoxin , the wonder drug does have an important vago mimetic action, to  reduce the heart rate .

Another  contentious issue   in SHIFT study  is , the Class 4 patients constituted <2% of the study population .It is ironical , these are the patients , one would  like to try a new rate control drugs like Ivabradine  , because we  are worried about beta blockers in this population  .A great opportunity was  lost as Ivabradine could have  been tried in this population.

We need a study  like this .

  • One to one comparison   of  beta blocker  and   Ivabradine  in cardiac failure  . Such a study will ever happen ? My guess is , it is  next to impossible !
  • Efficacy of  Ivabradine in patients with class 4  failure  , where beta blockers were contraindicated  or could not be administered.

Final message

Ivabradine , a new generation  negative chronotropic agent  is a great concept drug. But , the worthiness of this drug  is questionable , when we have  proven , well tolerated  drugs namely , the beta blockers to reduce the heart rate.. However , if the beta blockers are poorly tolerated  Ivabradine may be tried.Last , but not the least, never under-estimate the greatness of digoxin in heart failure.It is the only drug that has a positive  inotropic  properties coupled with  negative chronotropic action . Both benefits patients in CHF  . It can do wonders than any other drugs .(DIG trial was the most misunderstood by cardiologists!)

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The long standing controversy about diastolic heart failure is settled !

The perception that diastolic heart failure ( Now renamed as heart failure with preserved EF ) is less dangerous than systolic HF has been exposed by this land mark study by Owan TE, in 2006 (nejm) But unfortunately this information is not yet fully disseminated among the physician community. Hence this post, with due acknowledgment to NEJM & Owan et all.

Experts from the article

“The nosology of heart failure has been the
subject of much current debate, and some extreme
positions have been taken. The observation
that 22 to 29 percent of patients with diastolic
heart failure die within one year of hospital
discharge, and 65 percent die within five years,
is a reminder that we are facing a lethal condition,
regardless of its name. Owan et al. also
show that, in recent years, there has been little
improvement in survival rate among patients with
diastolic heart failure, in contrast to the improvement
in survival rate over time among patients
with systolic heart failure”

Have a look at the survival curve below, almost similar , surprise surprise ! DHF survival is not only worse ( in many ), than systolic CHF and further they respond poorly to treatment, compared to conventional systolic CHF .

Click below for the link to full text article

Short abstract :

Trends in prevalence and outcome of heart failure with preserved ejection fraction.

Cardiorenal Research Laboratory, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA.

BACKGROUND: The prevalence of heart failure with preserved ejection fraction may be changing as a result of changes in population demographics and in the prevalence and treatment of risk factors for heart failure. Changes in the prevalence of heart failure with preserved ejection fraction may contribute to changes in the natural history of heart failure. We performed a study to define secular trends in the prevalence of heart failure with preserved ejection fraction among patients at a single institution over a 15-year period. METHODS: We studied all consecutive patients hospitalized with decompensated heart failure at Mayo Clinic Hospitals in Olmsted County, Minnesota, from 1987 through 2001. We classified patients as having either preserved or reduced ejection fraction. The patients were also classified as community patients (Olmsted County residents) or referral patients. Secular trends in the type of heart failure, associated cardiovascular disease, and survival were defined. RESULTS: A total of 6076 patients with heart failure were discharged over the 15-year period; data on ejection fraction were available for 4596 of these patients (76 percent). Of these, 53 percent had a reduced ejection fraction and 47 percent had a preserved ejection fraction. The proportion of patients with the diagnosis of heart failure with preserved ejection fraction increased over time and was significantly higher among community patients than among referral patients (55 percent vs. 45 percent). The prevalence rates of hypertension, atrial fibrillation, and diabetes among patients with heart failure increased significantly over time. Survival was slightly better among patients with preserved ejection fraction (adjusted hazard ratio for death, 0.96; P=0.01). Survival improved over time for those with reduced ejection fraction but not for those with preserved ejection fraction. CONCLUSIONS: The prevalence of heart failure with preserved ejection fraction increased over a 15-year period, while the rate of death from this disorder remained unchanged. These trends underscore the importance of this growing public health problem. Copyright 2006 Massachusetts Medical Society.

Other interesting article

Heart failure with preserved ejection fraction: dangerous, elusive, and difficult.

Eur Heart J. 2008 Feb;29(3):339-47. Nielsen OW, Køber L, Torp-Pedersen C.

BMJ editorail 2009

http://www.bmj.com/cgi/content/full/338/jan27_1/b52?ijkey=c7a29d35dc9d9dddf7d0e75c5b8d05014315c564

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